Oncotarget

Research Papers:

This article has been corrected. Correction in: Oncotarget. 2019; 10:7189-7190.

MiR-1 downregulation correlates with poor survival in clear cell renal cell carcinoma where it interferes with cell cycle regulation and metastasis

Haibing Xiao, Jin Zeng, Heng Li, Ke Chen, Gan Yu, Junhui Hu, Kun Tang, Hui Zhou, Qihong Huang, Anping Li, Yi Li, Zhangqun Ye, Ji Wang and Hua Xu _

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Oncotarget. 2015; 6:13201-13215. https://doi.org/10.18632/oncotarget.3915

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Abstract

Haibing Xiao1,2,*, Jin Zeng1,2,*, Heng Li1,2, Ke Chen1,2, Gan Yu1,2, Junhui Hu1,2, Kun Tang1,2, Hui Zhou1,2, Qihong Huang3, Anping Li3, Yi Li1,2, Zhangqun Ye1,2, Ji Wang4 and Hua Xu1,2

1 Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

2 Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

3 The Wistar Institute, Philadelphia, PA, USA

4 Department of Cell Death and Cancer Genetics, The Hormel Institute, University of Minnesota, Austin, MN, USA

* Haibing Xiao and Jin Zeng contributed equally to this work

Correspondence to:

Hua Xu, email:

Ji Wang, email:

Keywords: miR-1, ccRCC, proliferation, metastasis

Received: December 02, 2014 Accepted: March 29, 2015 Published: April 23, 2015

Abstract

MicroRNAs (miRNA) that are strongly implicated in carcinogenesis have recently reshaped our understanding of the role of noncoding RNAs. Here, we focused on the function and molecular mechanism of miR-1 and its potential clinical application in clear cell renal cell carcinoma (ccRCC). First, miR-1 was significantly downregulated in 87.8% renal cancer samples compared with corresponding noncancerous tissues (NCT), which was significantly associated with clinical stage, T classification and poor overall survival. Functional study demonstrated that enforced overexpression of miR-1 in renal cancer cells inhibited proliferation and metastasis in vitro and in vivo. Conversely, miR-1 inhibitor silencing miR-1 expression promoted cell proliferation and metastasis in ccRCC. CDK4, CDK6, Caprin1 and Slug were each directly targeted for inhibition by miR-1 and restoring their expression reversed miR-1-mediated inhibition of cell cycle progression and metastasis. Taken together, our findings established a tumor suppressive role for miR-1 in the progression of ccRCC by targeting CDK4, CDK6, Caprin1 and Slug and suggested miR-1 can be served as a novel potential therapeutic target for ccRCC.


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